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Thal Amyloid Stages Do Not Significantly Impact the Correlation Between Neuropathological Change and Cognition in the Alzheimer Disease Continuum.
J Neuropathol Exp Neurol 2016; 75(6):516-26JN

Abstract

The 2012 neuropathological criteria for the diagnosis of Alzheimer disease (AD) summarize the extent of AD neuropathological change with an ABC score, which is a composite of the Thal stage of amyloid deposition (A), the Braak stage of neurofibrillary tangles (NFTs) (B), and the CERAD neuritic plaque score (C). NFTs and neuritic plaques are well-established contributors to cognitive impairment, but whether the Thal amyloid stage independently predicts antemortem cognition remains unknown. We used the National Alzheimer's Coordinating Center autopsy data set to build adjacent-categories logit regression models with CDR-SOB and Mini-Mental State Examination (MMSE) scores as cognitive outcome variables. Increasing CERAD scores were independently associated with higher CDR-SOB scores, whereas increasing Braak NFT stages predicted both higher CDR-SOB and lower MMSE scores. Increasing Thal amyloid stages were not significantly independently associated with either outcome measure. Increasing ABC scores predicted higher CDR-SOB and lower MMSE scores. These results raise the possibility that Thal amyloid stages do not substantially contribute to predicting antemortem cognition compared to CERAD neuritic plaque scores and Braak NFT stages, and suggest that the diffuse amyloid deposits participating in the assignment of Thal amyloid stages are neutral with respect to clinically detectable cognitive and functional changes.

Authors+Show Affiliations

From the Department of Neurology of the University of Iowa Hospitals & Clinics, Iowa City, Iowa (AS-P); Department of Biostatistics and Epidemiology of the University of Massachusetts, Amherst, Massachusetts (JQ); Massachusetts General Hospital Biostatistics Center, Boston, Massachusetts (AM); Department of Biostatistics, University of Washington, Seattle, Washington (SEM); Department of Pathology, School of Medicine of the University of Washington, Seattle, Washington (TJM); C. S. Kubik Laboratory for Neuropathology of the Massachusetts General Hospital (MPF), Department of Neurology of the Massachusetts General Hospital, Boston, Massachusetts (BTH); Department of Biostatistics of the Harvard T. H. Chan School of Public Health, Boston, Massachusetts (RAB); and Massachusetts Alzheimer Disease Research Center, Charlestown, Massachusetts (MPF, RAB, BTH).From the Department of Neurology of the University of Iowa Hospitals & Clinics, Iowa City, Iowa (AS-P); Department of Biostatistics and Epidemiology of the University of Massachusetts, Amherst, Massachusetts (JQ); Massachusetts General Hospital Biostatistics Center, Boston, Massachusetts (AM); Department of Biostatistics, University of Washington, Seattle, Washington (SEM); Department of Pathology, School of Medicine of the University of Washington, Seattle, Washington (TJM); C. S. Kubik Laboratory for Neuropathology of the Massachusetts General Hospital (MPF), Department of Neurology of the Massachusetts General Hospital, Boston, Massachusetts (BTH); Department of Biostatistics of the Harvard T. H. Chan School of Public Health, Boston, Massachusetts (RAB); and Massachusetts Alzheimer Disease Research Center, Charlestown, Massachusetts (MPF, RAB, BTH).From the Department of Neurology of the University of Iowa Hospitals & Clinics, Iowa City, Iowa (AS-P); Department of Biostatistics and Epidemiology of the University of Massachusetts, Amherst, Massachusetts (JQ); Massachusetts General Hospital Biostatistics Center, Boston, Massachusetts (AM); Department of Biostatistics, University of Washington, Seattle, Washington (SEM); Department of Pathology, School of Medicine of the University of Washington, Seattle, Washington (TJM); C. S. Kubik Laboratory for Neuropathology of the Massachusetts General Hospital (MPF), Department of Neurology of the Massachusetts General Hospital, Boston, Massachusetts (BTH); Department of Biostatistics of the Harvard T. H. Chan School of Public Health, Boston, Massachusetts (RAB); and Massachusetts Alzheimer Disease Research Center, Charlestown, Massachusetts (MPF, RAB, BTH).From the Department of Neurology of the University of Iowa Hospitals & Clinics, Iowa City, Iowa (AS-P); Department of Biostatistics and Epidemiology of the University of Massachusetts, Amherst, Massachusetts (JQ); Massachusetts General Hospital Biostatistics Center, Boston, Massachusetts (AM); Department of Biostatistics, University of Washington, Seattle, Washington (SEM); Department of Pathology, School of Medicine of the University of Washington, Seattle, Washington (TJM); C. S. Kubik Laboratory for Neuropathology of the Massachusetts General Hospital (MPF), Department of Neurology of the Massachusetts General Hospital, Boston, Massachusetts (BTH); Department of Biostatistics of the Harvard T. H. Chan School of Public Health, Boston, Massachusetts (RAB); and Massachusetts Alzheimer Disease Research Center, Charlestown, Massachusetts (MPF, RAB, BTH).From the Department of Neurology of the University of Iowa Hospitals & Clinics, Iowa City, Iowa (AS-P); Department of Biostatistics and Epidemiology of the University of Massachusetts, Amherst, Massachusetts (JQ); Massachusetts General Hospital Biostatistics Center, Boston, Massachusetts (AM); Department of Biostatistics, University of Washington, Seattle, Washington (SEM); Department of Pathology, School of Medicine of the University of Washington, Seattle, Washington (TJM); C. S. Kubik Laboratory for Neuropathology of the Massachusetts General Hospital (MPF), Department of Neurology of the Massachusetts General Hospital, Boston, Massachusetts (BTH); Department of Biostatistics of the Harvard T. H. Chan School of Public Health, Boston, Massachusetts (RAB); and Massachusetts Alzheimer Disease Research Center, Charlestown, Massachusetts (MPF, RAB, BTH).From the Department of Neurology of the University of Iowa Hospitals & Clinics, Iowa City, Iowa (AS-P); Department of Biostatistics and Epidemiology of the University of Massachusetts, Amherst, Massachusetts (JQ); Massachusetts General Hospital Biostatistics Center, Boston, Massachusetts (AM); Department of Biostatistics, University of Washington, Seattle, Washington (SEM); Department of Pathology, School of Medicine of the University of Washington, Seattle, Washington (TJM); C. S. Kubik Laboratory for Neuropathology of the Massachusetts General Hospital (MPF), Department of Neurology of the Massachusetts General Hospital, Boston, Massachusetts (BTH); Department of Biostatistics of the Harvard T. H. Chan School of Public Health, Boston, Massachusetts (RAB); and Massachusetts Alzheimer Disease Research Center, Charlestown, Massachusetts (MPF, RAB, BTH).From the Department of Neurology of the University of Iowa Hospitals & Clinics, Iowa City, Iowa (AS-P); Department of Biostatistics and Epidemiology of the University of Massachusetts, Amherst, Massachusetts (JQ); Massachusetts General Hospital Biostatistics Center, Boston, Massachusetts (AM); Department of Biostatistics, University of Washington, Seattle, Washington (SEM); Department of Pathology, School of Medicine of the University of Washington, Seattle, Washington (TJM); C. S. Kubik Laboratory for Neuropathology of the Massachusetts General Hospital (MPF), Department of Neurology of the Massachusetts General Hospital, Boston, Massachusetts (BTH); Department of Biostatistics of the Harvard T. H. Chan School of Public Health, Boston, Massachusetts (RAB); and Massachusetts Alzheimer Disease Research Center, Charlestown, Massachusetts (MPF, RAB, BTH).From the Department of Neurology of the University of Iowa Hospitals & Clinics, Iowa City, Iowa (AS-P); Department of Biostatistics and Epidemiology of the University of Massachusetts, Amherst, Massachusetts (JQ); Massachusetts General Hospital Biostatistics Center, Boston, Massachusetts (AM); Department of Biostatistics, University of Washington, Seattle, Washington (SEM); Department of Pathology, School of Medicine of the University of Washington, Seattle, Washington (TJM); C. S. Kubik Laboratory for Neuropathology of the Massachusetts General Hospital (MPF), Department of Neurology of the Massachusetts General Hospital, Boston, Massachusetts (BTH); Department of Biostatistics of the Harvard T. H. Chan School of Public Health, Boston, Massachusetts (RAB); and Massachusetts Alzheimer Disease Research Center, Charlestown, Massachusetts (MPF, RAB, BTH). bhyman@mgh.harvard.edu.

Pub Type(s)

Journal Article
Multicenter Study
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

27105663

Citation

Serrano-Pozo, Alberto, et al. "Thal Amyloid Stages Do Not Significantly Impact the Correlation Between Neuropathological Change and Cognition in the Alzheimer Disease Continuum." Journal of Neuropathology and Experimental Neurology, vol. 75, no. 6, 2016, pp. 516-26.
Serrano-Pozo A, Qian J, Muzikansky A, et al. Thal Amyloid Stages Do Not Significantly Impact the Correlation Between Neuropathological Change and Cognition in the Alzheimer Disease Continuum. J Neuropathol Exp Neurol. 2016;75(6):516-26.
Serrano-Pozo, A., Qian, J., Muzikansky, A., Monsell, S. E., Montine, T. J., Frosch, M. P., ... Hyman, B. T. (2016). Thal Amyloid Stages Do Not Significantly Impact the Correlation Between Neuropathological Change and Cognition in the Alzheimer Disease Continuum. Journal of Neuropathology and Experimental Neurology, 75(6), pp. 516-26. doi:10.1093/jnen/nlw026.
Serrano-Pozo A, et al. Thal Amyloid Stages Do Not Significantly Impact the Correlation Between Neuropathological Change and Cognition in the Alzheimer Disease Continuum. J Neuropathol Exp Neurol. 2016;75(6):516-26. PubMed PMID: 27105663.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Thal Amyloid Stages Do Not Significantly Impact the Correlation Between Neuropathological Change and Cognition in the Alzheimer Disease Continuum. AU - Serrano-Pozo,Alberto, AU - Qian,Jing, AU - Muzikansky,Alona, AU - Monsell,Sarah E, AU - Montine,Thomas J, AU - Frosch,Matthew P, AU - Betensky,Rebecca A, AU - Hyman,Bradley T, Y1 - 2016/04/22/ PY - 2016/01/27/received PY - 2016/02/28/accepted PY - 2016/4/24/entrez PY - 2016/4/24/pubmed PY - 2017/6/24/medline KW - ABC score KW - Alzheimer disease KW - Amyloid plaques KW - National Alzheimer’s Coordinating Center KW - Neuritic plaques KW - Neurofibrillary tangles KW - Thal stages. SP - 516 EP - 26 JF - Journal of neuropathology and experimental neurology JO - J. Neuropathol. Exp. Neurol. VL - 75 IS - 6 N2 - The 2012 neuropathological criteria for the diagnosis of Alzheimer disease (AD) summarize the extent of AD neuropathological change with an ABC score, which is a composite of the Thal stage of amyloid deposition (A), the Braak stage of neurofibrillary tangles (NFTs) (B), and the CERAD neuritic plaque score (C). NFTs and neuritic plaques are well-established contributors to cognitive impairment, but whether the Thal amyloid stage independently predicts antemortem cognition remains unknown. We used the National Alzheimer's Coordinating Center autopsy data set to build adjacent-categories logit regression models with CDR-SOB and Mini-Mental State Examination (MMSE) scores as cognitive outcome variables. Increasing CERAD scores were independently associated with higher CDR-SOB scores, whereas increasing Braak NFT stages predicted both higher CDR-SOB and lower MMSE scores. Increasing Thal amyloid stages were not significantly independently associated with either outcome measure. Increasing ABC scores predicted higher CDR-SOB and lower MMSE scores. These results raise the possibility that Thal amyloid stages do not substantially contribute to predicting antemortem cognition compared to CERAD neuritic plaque scores and Braak NFT stages, and suggest that the diffuse amyloid deposits participating in the assignment of Thal amyloid stages are neutral with respect to clinically detectable cognitive and functional changes. SN - 1554-6578 UR - https://www.unboundmedicine.com/medline/citation/27105663/Thal_Amyloid_Stages_Do_Not_Significantly_Impact_the_Correlation_Between_Neuropathological_Change_and_Cognition_in_the_Alzheimer_Disease_Continuum_ L2 - https://academic.oup.com/jnen/article-lookup/doi/10.1093/jnen/nlw026 DB - PRIME DP - Unbound Medicine ER -